Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

SALL4 ensures oocytes maturation by modulating DNA methylation and histone modifications

ABSTRACT: SALL4 ensures oocytes maturation by modulating DNA methylation and histone modifications

PROVIDER: PRJNA335644 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

SALL4 ensures oocytes maturation by modulating DNA methylation and histone modifications (RRBS)

Project description:Splat-like 4 (Sall4) plays important roles in maintaining pluripotency of embryonic stem cells and in various developmental processes. Here, we find that the SALL4 null oocytes fail to undergo maturation to form fully-grown oocytes (FGOs) and subsequent meiosis resumption. We further discover that the loss of maternal SALL4 causes failure in establishment of DNA methylation. Moreover, we demonstrate that SALL4 modulates H3K4me3 and H3K27me3 modifications by regulating the expression of Kdm5b, Kdm6a and Kdm6b. Taken together, SALL4 plays pivotal roles in oocyte epigenetic maturation.

2017-03-07 | GSE84923 | GEO

SALL4 ensures oocytes maturation by modulating DNA methylation and histone modifications (RNA-Seq)

2017-03-07 | GSE84922 | GEO

SALL4 ensures oocytes maturation by modulating DNA methylation and histone modifications

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-03-07 | GSE84924 | GEO

Mus musculus

Project description:SALL4 ensures oocytes maturation by modulating DNA methylation and histone modifications (RRBS)

| PRJNA335648 | ENA

Mus musculus

Project description:SALL4 ensures oocytes maturation by modulating DNA methylation and histone modifications (RNA-Seq)

| PRJNA335647 | ENA

Maternal Sall4 Is Indispensable for Epigenetic Maturation of Mouse Oocytes.

Project description: Not available

| S-EPMC5290953 | biostudies-literature

A novel role of stem cell factor SALL4 as an oncofetal protein in hepatocellular carcinoma

Project description:Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths worldwide. Treatment of HCC remains abysmal; discovery of novel pathways implicated in hepatocarcinogenesis is needed for more effective therapeutics. SALL4 is a stem cell factor essential for the maintenance of embryonic stem cell self-renewal properties and expressed in fetal liver, but silenced in normal adult liver. We observed that expression of SALL4 in murine liver in a transgenic model led to development of HCC. In humans, SALL4 is re-expressed as an oncofetal protein in a subgroup of HCC patients with unfavorable prognoses. Loss-of-function studies demonstrated that SALL4 is essential for human HCC cell survival and tumorigenicity. We demonstrated that a peptide can block the oncogenic function of SALL4 in HCC by modulating the PTEN/AKT pathway. Our findings reveal a novel role of SALL4 in HCC with important implications for understanding disease mechanisms and development of innovative therapeutics. Cultured cells from HCC cell line SNU-398 with scrambled or SALL4 shRNA knockdown were used for RNA extraction and hybridization on Affymetrix microarrays.

2012-02-22 | E-GEOD-35965 | biostudies-arrayexpress

Expression profile of Sall4-null ES cells and Sall4 heterozygous ES cells

Project description:Sall4 is a mouse homolog of a causative gene of the autosomal dominant disorder known as Okihiro syndrome. We previously showed that Sall4 absence leads to lethality during peri-implantation and that Sall4-null embryonic stem (ES) cells proliferate poorly with intact pluripotency when cultured on feeder cells. However, a subsequent report indicated that shRNA-mediated Sall4 inhibition in ES cells led to a severe reduction in Oct3/4 and a secondary increase in Cdx2, which resulted in complete differentiation into the trophectoderm when cultured in the feeder-free condition. So we profiled gene expression changes when Sall4 is deleted in ES cells in the presence or absence of feeder cells. key word: embryonic stem (ES) cell, Sall4, feeder

2009-04-01 | GSE14219 | GEO

A novel role of stem cell factor SALL4 as an oncofetal protein in hepatocellular carcinoma

2012-02-22 | GSE35965 | GEO

SALL4 Occupany in mESCs by Cut & Run

Project description:High confidence SALL4 targets were identified in mESCs by performing Cut&Run on SALL4 Flox/Flox and SALL4 -/- cells. We validated a commercially available antibody that specifically recognizes SALL4 protein.

2022-12-08 | GSE203303 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data